Objective: To test the hypothesis that different preceding infections influ
ence the neurophysiologic classification and clinical features of Guillain-
Barre syndrome (GBS). Methods: We tested pretreatment sera, 7 +/- 3 (mean /- SD) days from onset, from 229 patients with GBS in a multicenter trial o
f plasma exchange and immunoglobulin, for serological markers of infection,
adhesion molecules, and cytokine receptors, and compared these with neurop
hysiologic and clinical features. Results: Recent infection by Campylobacte
r jejuni was found in 53 patients (23%), cytomegalovirus in 19 (8%), and Ep
stein-Barr virus in four (2%). Patients with C, jejuni infection were more
likely than others to have neurophysiologic criteria of axonal neuropathy o
r inexcitable nerves, antiganglioside GM, antibodies, pure motor GBS, lower
CSF protein, and worse outcome, Patients with cytomegalovirus infection we
re younger and more likely than others to have raised serum concentrations
of molecules important in T lymphocyte activation and migration, soluble in
tercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion m
olecule-1 (sVCAM-1), soluble leukocyte selectin, and soluble interleukin-2
receptor (sIL-2R). Concentrations of sICAM-1 and soluble tumor necrosis fac
tor receptor were higher in patients with inexcitable nerves than those wit
h demyelinating neurophysiology. Logistic regression analysis showed death
or inability to walk unaided at 48 weeks were associated with diarrhea, ine
xcitable nerves, severe arm weakness, age over 50, raised sIL-2R concentrat
ion and absence of immunoglobulin (Ig) M antiganglioside GM, antibodies. Co
nclusions: Subtypes of GBS defined by preceding infections were only approx
imately associated with different patterns of clinical, neurophysiologic, a
nd immunologic features. A single infectious agent caused more than one typ
e of pathology in GBS, implying interaction with additional host factors. M
ost patients had no identified infection.